Epidemiological, migration, intervention, and genetic studies in humans and animals provide very strong evidence of a causal link between high salt intake and high blood pressure. The mechanisms by which dietary salt increases arterial pressure are not fully understood, but they seem related to the inability of the kidneys to excrete large amounts of salt. From an evolutionary viewpoint, the human species is adapted to ingest and excrete <1 g of salt per day, at least 10 times less than the average values currently observed in industrialized and urbanized countries. Independent of the rise in blood pressure, dietary salt also increases cardiac left ventricular mass, arterial thickness and stiffness, the incidence of strokes, and the severity of cardiac failure. Thus chronic exposure to a high-salt diet appears to be a major factor involved in the frequent occurrence of hypertension and cardiovascular diseases in human populations.

Links between dietary salt intake, renal salt handling, blood pressure, and cardiovascular diseases.

This article summarizes anatomical, neurophysiological, pharmacological, and brain imaging studies in humans and animals that have provided insights into the neural circuitry and neurotransmitter mechanisms controlling the lower urinary tract. The functions of the lower urinary tract to store and periodically eliminate urine are regulated by a complex neural control system in the brain, spinal cord, and peripheral autonomic ganglia that coordinates the activity of smooth and striated muscles of the bladder and urethral outlet. The neural control of micturition is organized as a hierarchical system in which spinal storage mechanisms are in turn regulated by circuitry in the rostral brain stem that initiates reflex voiding. Input from the forebrain triggers voluntary voiding by modulating the brain stem circuitry. Many neural circuits controlling the lower urinary tract exhibit switch-like patterns of activity that turn on and off in an all-or-none manner. The major component of the micturition switching circuit is a spinobulbospinal parasympathetic reflex pathway that has essential connections in the periaqueductal gray and pontine micturition center. A computer model of this circuit that mimics the switching functions of the bladder and urethra at the onset of micturition is described. Micturition occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary micturition, leading to urinary incontinence. Neuroplasticity underlying these developmental and pathological changes in voiding function is discussed.

/pdf/neural-control-of-the-lower-urinary-tract-2ombjmcwkx.pdf

Neural Control of the Lower Urinary Tract

Epithelial sodium channel (ENaC) family: Phylogeny, structure-function, tissue distribution, and associated inherited diseases.

The uroepithelium sits at the interface between the urinary space and underlying tissues, where it forms a high-resistance barrier to ion, solute, and water flux, as well as pathogens. However, the uroepithelium is not simply a passive barrier; it can modulate the composition of the urine, and it functions as an integral part of a sensory web in which it receives, amplifies, and transmits information about its external milieu to the underlying nervous and muscular systems. This review examines our understanding of uroepithelial regeneration and how specializations of the outermost umbrella cell layer, including tight junctions, surface uroplakins, and dynamic apical membrane exocytosis/endocytosis, contribute to barrier function and how they are co-opted by uropathogenic bacteria to infect the uroepithelium. Furthermore, we discuss the presence and possible functions of aquaporins, urea transporters, and multiple ion channels in the uroepithelium. Finally, we describe potential mechanisms by which the uroepithelium can transmit information about the urinary space to the other tissues in the bladder proper.

Cell biology and physiology of the uroepithelium.

The mammalian urinary bladder epithelium (urothelium) performs the important function of storing urine for extended periods, while maintaining the urine composition similar to that delivered by the kidneys. The urothelium possesses four properties to perform this function. First, it offers a minimum epithelial surface area-to-urine volume; this reduces the surface area for passive movement of substances between lumen and blood. Second, the passive permeability of the apical membrane and tight junctions is very low to electrolytes and nonelectrolytes. Third, the urothelium has a hormonally regulated sodium absorptive system; thus passive movement of sodium from blood to urine is countered by active sodium reabsorption. Last, the permeability properties of the apical membrane and tight junctions of the urothelium are not altered by most substances found in the urine or blood. The importance of the barrier function of the urothelium is illustrated by infectious cystitis. The loss of the barrier function results in the movement of urinary constituents into the lamina propria and underlying muscle layers, resulting in suprapubic and lower back pain and frequent, urgent, and painful voiding.

https://www.physiology.org/doi/pdf/10.1152/ajprenal.2000.278.6.F867

Everything you wanted to know about the bladder epithelium but were afraid to ask

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Expression and localization of epithelial sodium channel in mammalian urinary bladder

Functional polymorphism in the carboxyl terminus of the α-subunit of the human epithelial sodium channel

Multiple epithelial Na+ channel domains participate in subunit assembly

in mammalian urinary bladder Expression and localization of epithelial sodium channel